2019B MCQ's Flashcards
- Dental damage risk to be determined in your department. 100 cases reviewed, zero cases of dental damage. What is the 95% confidence interval? a) 1/100 b) 2/100 c) 3/100 d) 5/100 e) 9/100 f) 10/100
Answer = c) 3/100 • Confidence intervals when no events are observed o Rule of threes for when no events are observed in a group, then the upper confidence interval limit for the number of events is three, & for the risk (in a sample size N) is 3/N o The value 3 coincides with the upper limit of a one-tailed 95% confidence interval from the Poisson distribution • Rule of thumb for estimating lower confidence interval in trials w small event rates o The two-tailed upper 95% CI for 0, 1, 2, 3, and 4 observed events are 3, 5, 7, 9, and 10 events, respectively o The upper 95% CI for the event rate is thus given by 3/n, 5/n, 7/n, 9/n, and 10/n, respectively, where n = number involved in the study
Response surface modelling evaluates a) Combined response when given two drugs b) No other options remembered
Answer = a) Combined response when given two drugs • Response surfaces can describe anaesthetic interactions, even those btwn agonists, partial agonists, competitive antagonists, & inverse agonists • Application of response-surface methods permits characterisation of the full concentration-response relation, & therefore can be used to develop practical guidelines for optimal drug dosing
- After stopping smoking, when does immune response return to normal? a) 2 weeks b) 8 weeks c) 6 months d) 3 months e) 1 year
Answer = c) 6 months • PS12 timing of smoking cessation + physiological effects o 1 day = Decreased carboxyHb + nicotine levels!improves tissue O2 delivery o 3 weeks = Improves wound healing o 6-8 weeks = Same vol of sputum as non-smokers + improves lung fx o 6 months = Immune fx significantly improved
- Lung USS – Picture had no B lines (comet tails). What does this indicate? a) Pneumothorax b) Normal lung c) Interstitial fluid d) Pulmonary oedema e) Pleural effusion
Answer = a) Pneumothorax • On lung USS o Lung sliding shows movement of parenchyma relative to pleura ! Normal o A lines = Horizontal hyperechoic lines that are reverberation artefact from pleura!Normal o Comet tails = Short, vertical hyperechoic lines that descend partially down the screen from pleura!Normal o B lines = Vertical hyperechoic columns descending all the way (like a flashlight beam)!Interstitial oedema (if bilateral) // Pneumonia // Contusion (if unilateral)!Abnormal
- The most common cause of airway compromise following anterior cervical spine fusion is a) Haematoma b) Abscess c) Oedema d) Failure of surgical implant / fusion e) Vocal cord palsy
Answer = c) Oedema ***2019A repeat • Haematoma occurs less freq than tissue oedema • Bilateral VC palsy causing airway compromise is also rare CEACCP o Some degree of airway obstruction is NOT uncommon after anterior cervical surgery o Sometimes secondary to haematoma, but in many cases, it is secondary to tissue swelling (oedema) o Usu presents w.in 6hrs, but can occur later o Airway obstruction is particularly likely after combined anterior-posterior cervical surgery Blue book 2017 article – - Airway Mx after cervical spine surgery o Wide rate of post-op airway compromise ! 1-3% o Up to 6% re-intubation rate o Due to upper airway oedema (UAO) “ Immediately = Due to haematoma formation + CSF leak + accumulation “ Days later = UAO due to pre-vertebral tissue swelling!Danger as onset can be insidious in ward environment, leading to late recognition o RFs for airway complications post C-spine surgery “ Combined anterior-posterior approach “ Pre-existing myelopathy “ Prolonged operating time >5hrs “ Est blood loss >300mL “ Multiple cervical levels, 3+ “ Surg involving C2 fusion, or C1 odontoid peg “ Pre-existing pulmonary disease o Mx “ Perform surg in suitable facility w 24hr anaesthetic service for re-intubation + ICU if necessary “ Delay extubation if combined AP approach + 2 or more above RFs to allow post-op swelling to resolve === “ Secure airway w minimal pharyngeal trauma!AFOI or best tech “ Delay extubation if • Halo-thoracic brace insitu • OSA • Pre-existing resp disease (COPD) • Gross facial oedema at end of case “ High risk extubation protocol • Use AEC • Extubate w close monitoring in ICU setting
- The dose of Hydrocortisone equivalent to Dexamethasone 8mg, with regards to glucocorticoid activity a) 12mg b) 25mg c) 50mg d) 100mg e) 200mg
Answer = e) 200mg • Dexamethasone has 25x glucocorticoid potency of Hydrocortisone • Therefore 8mg Dex = 200mg Hydrocort • Dex 4 = Pred 25 = Hydrocort 100
- The reason for increased dose requirement of Rocuronium after burns is a) Increased alpha 1 acid glycoprotein binding b) Downregulation of AChR c) Upregulation of AChR d) Increased number of AChR e) Incerased sensitivity of AChR f) Increased albumin binding g) Increased acetylcholinesterase production
Answer = d) Increased number of AChR ??? c) Upregulation of AChR 2019A repeat • Resistance to neuromuscular effects of NDNMBs after major burns takes several days to develop + may persist for several months after wound healing • This resistance is observed when burn injury >20% of TBSA + is manifested as a slower onset of paralysis, inadequate paralysis, or faster recovery, when normal doses are administered to these pts • The peri-junctional proliferation + expression of immature, foetal type, or both alpha 7 neuronal AChRs on the mm memb probably plays a major role in the altered neuromuscular pharmacodynamics • Muscle relaxant pharmacology is sig + consistently altered after burn injury • In burn pts, exposure to Sux can cause an exaggerated hyperkalaemic response, which can induce cardiac arrest • The current recommendation is to avoid Sux in pts 48hrs after burn injury • An inc in the number of etrajunctional AChRs that release K during depolarisation w Sux is the cause for inc’d hyperkalaemia • There is also a concomitant dec’d sensitivity to neuromuscular effects of NDNMBs • ~3-7 days after burn injury, the dose of NDNMBs req’d to achieve effective paralysis can be substantially inc’d • The aetiology of the altered response to NDNMBs is multifactorial === o Up-regulation of AChRs, including up-regulation of foetal + alpha 7 (neuronal type) AChRs at mm memb o Inc’d binding to AAG + enhanced renal + hepatic elimination of NDNMBs
- A 30yo 38 week pregnant woman with severe idiopathic pulmonary hypertension presents for elective lower segment caesarean section. The most important thing to avoid during her anaesthetic management is a) An epidural b) Hypocarbia c) Decreased systemic vascular resistance d) Tachycardia e) Nitrous oxide
Answer = c) or e), not sure which would be the MOST important thing to avoid • N2O is pretty much said to be avoided in any text or recent guideline to managing pHTN, due to effects of inc’ing PVR o But, there are some old studies from the 80’s, 90’s, which showed that although there is a statistically sig inc in PVR, the clinical consequences weren’t really sig • A drop in SVR per se might not be that bad, but anything that drops SVR almost inevitably drops BP + VR to the Right heart from venodilation, which does have much more serious consequences, + can easily precipitate pulmonary hypertensive crisis, as opposed to the N2O, so I want to lean towards this as the MOST important thing to avoid • But if you purely drop your SVR, I don’t think it would have a huge impact • If the Qu asked about drop in BP or Right heart preload, then definitely that would be the answer over N2O I think
- Warm ischaemic time for lungs in transplant
a) 30 min
b) 45 min
c) 60 min
d) 90 min
e) 120 min
Answer = d) 90 min
• Warm ischaemic times
o 30 mins = Liver, Pancreas
o 60 mins = Kidneys
o 90 mins = Lungs
What is this ECG?
a) HOCM
b) LVH
c) Acute inferior ischaemia
d) Viral myocarditis
e) Bisfascicular block
Answer = b) LVH
Main abnormality here is global T wave inversion in all leads, & voltage criteria for LVH
Not sure if this is diagnostic for one of the options, so maybe b) LVH?
Not sure if viral myocarditis can look like this
HOCM is a/w LVH + classically “dagger” Q waves in inferolateral leads (deep, short duration Q waves – usu deeper + shorter
than post-ischaemia Q waves)
Inferior ischaemia would be a/w Q waves, TWI in leads II, III, aVF
Bifascicular block would show RBBB (RSR pattern in V1-2) + LAD + dominant S wave in aVF (to suggest LAFB)
- Hypothermia in a neonate is best prevented by addressing…
a) Conduction from skin
b) Convection from skin
c) Evaporation from skin
d) Evaporation from respiration
e) Radiation from skin
Answer = e) Radiation from skin
- Greatest source of heat loss in neonates (similar to adults in OT environment) is through radiation
- Preventive tech focus on nullifying temp gradient from surrounding air to neonate, eg wrap baby, use heat lamp •
- Evaporative losses may be insensible (skin + breathing), or sensible (sweating)
- Other factors that contribute to evaporative losses are the newborn’s surface area, vapor pressure + air velocity
- This is the greatest source of heat loss AT BIRTH
- Radiation is where the newborn is near cool objects, walls, tables, cabinets, w.out actually being in contact w them o The t/f of heat btwn solid surfaces that are not touching
- Factors that affect heat change due to radiation are temp gradient btwn 2 surfaces, SA of solid surfaces, & distance btwn solid surfaces
- This is the greatest source of heat loss AFTER BIRTH
- Definition of septic shock is sepsis with adequate fluid resuscitation, requiring vasopressor to maintain a mean arterial pressure of
a) 55mmHg and lactate >2
b) 55mmHg and lactate >4
c) 65mmHg and lactate >2
d) 65mmHg and lactate >4
e) Another option
Answer = c) MAP >/= 65mmHg + lactate >2mmol/L
3rd international consensus definition for Sepsis + Septic shock (Sepsis 3) – JAMA 2016
-
Sepsis = Life-threatening organ dysfx, caused by a dysregulated host response to infection
- Organ dysfx represented by inc’d Sequential Organ Failure Assessment (SOFA) score of 2 points or more !a/w in-hospital mortality >10%
-
Septic shock = Subset of sepsis, in which particularly profound circulatory, cellular + metabolic abN are a/w greater risk of mortality, than w sepsis alone
- Vasopressor req’d to maintain MAP >/=65mmHg + serum lactate >2mmol/L, in absence of hypovolaemia ⇒ a/w hospital mortality >40%
-
qSOFA = quickSOFA = New bedside clinical score relevant to adults w suspected infection
- Rapidly identifies those at risk
- If have 2 or more = more likely to have poor outcomes typical of sepsis
- 3 components =
- RR >/= 22/min
- Altered mentation
- SBP = 100mmHg
- A 65yo man is having a TKR. Which blood tests, in addition to FBC are needed to reduce his transfusion requirements?
a) Coagulation profile
b) Iron studies + coagulation profile
c) Iron studies + CRP + renal function
d) Coagulation + liver + renal function
e) Iron studies + coagulation profile + CRP
Answer = e) Iron studies + coagulation profile + CRP
- Not v clear what they want*
- Fe studies + CRP would identify IDA + allow pre-op optimisation w Fe supplementation!dec’s transfusion req’s*
- Coagulation profile would identify any coagulopathy that may worsen intra-op bleeding. This could be corrected to dec*
- intra-op blood loss!dec transfusion req’s*
- Can’t find any reason why renal fx would affect transfusion req’s*
- Metabolism of Esmolol is by
a) Plasma esterases
b) Hepatic metabolism
c) Pseudocholinesterase
d) Red cell esterases
e) Hofmann degradation
f) Renal excretion
Answer = d) Red cell esterases
• Rapidly metabolised to inactive form by hydrolysis of ester linkage, chiefly by red blood cell esterases, and NOT by plasma cholinesterase, or red cell memb acetylcholinesterase
- Predominant feature of propofol infusion syndrome
a) Hepatomegaly
b) Liver failure
c) Bradycardia
d) Rhabdomyolysis
Answer = c) Bradycardia
• Can be a/w all of the above, but cardinal feature = refractory bradycardia, which may progress to asystole
CEACCP - https://academic.oup.com/bjaed/article/13/6/200/246704#2902188
LITFL - https://litfl.com/propofol-related-infusion-syndrome/
Acute refractory bradycardia progressing to asystole and one or more of the following: metabolic acidosis; rhabdomyolysis, hyperlipidaemai, and enlarged or fatty liver.
Mechanism: ?direct mitochondrial respiratory chain inhibition OR impaired fatty acid metabolism.
At risk with:
- high dose, long duraiton of props >4mg/kg/hr for 48h.
- younger age
- acute neurological injury
- low carbohydrate intake
- catecholamine infusion
- corticosteroid infusions
Clincal features:
- Primigravida 37/40 gestation with uncontrolled pre-eclampsia and BP 160/110. Her haemodynamics will be
a) High cardiac output, high SVR
b) High cardiac output, low SVR
c) Normal cardiac output, high SVR
d) Normal cardiac output, increased diastolic pressure
e) Low cardiac output, high SVR
Answer = Potentially c) Normal cardiac output, high SVR. e) if pre-term pre-eclamptic, Low cardiac output, high SVR
- Depends on actual Qu – pre-term / early onset pre-eclampsia <34/40 is v clearly low CO w high SVR, esp if a/w IUGR
- But there’s some suggestion that late-onset pre-eclampsia >34/40 is a/w normal-high CO, high SVR from 2019 article
- Certainly, term pre-eclampsia is a/w higher CO + lower SVR than pre-term pre-eclampsia